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pubmed-article:21321117pubmed:abstractTextIL-32 was recently identified as a proinflammatory cytokine that is induced by IL-18 in natural killer (NK) cells and is highly correlated with inflammatory disorders. However, the relationship between IL-32 and tumor progression is still unknown. In this study, we investigated whether overexpression of IL-32 affects susceptibility of chronic myeloid leukemia (CML) cells to NK cells. Interestingly, IL-32?-overexpressing CML cell lines, K562, Kcl22, and BV173, showed higher NK cell-mediated killing. Flow cytometry analysis revealed that overexpression of IL-32? induced increased expression of Fas and UL16-binding protein 2 (ULBP2) in CML cells. The direct relationship between overexpression of surface molecules by IL-32? and increased NK cell-mediated killing was confirmed by Fas or ULBP2 siRNA transfection. IL-32?-induced Fas and ULBP2 expression are regulated p38 MAPK. In addition, the transcription factor Ets1 plays a key role in ULBP2 specific expression by IL-32? overexpression in ULBP family members. Taken together, these data show that IL-32? stimulates Fas and ULBP2 expression via activation of p38 MAPK, which increases NK susceptibility of CML cells. Enhanced NK cell susceptibility of CML cells by IL-32? overexpression may improve the efficiency of NK cell-based immunotherapy.lld:pubmed
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pubmed-article:21321117pubmed:articleTitleOverexpression of IL-32alpha increases natural killer cell-mediated killing through up-regulation of Fas and UL16-binding protein 2 (ULBP2) expression in human chronic myeloid leukemia cells.lld:pubmed
pubmed-article:21321117pubmed:affiliationDepartment of Life Science, Sookmyung Women's University, and Konkuk University Hospital, Seoul 140-742, Republic of Korea.lld:pubmed
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